tbuckley/cabot-search huggingface dataset:
POS0684 INFLAMMATION IS ASSOCIATED WITH INCIDENT HYPERTENSION IN PATIENTS WITH AXIAL SPONDYLOARTHRITIS: A LONGITUDINAL COHORT STUDY
Authors: J. L. H. Shi, S. H. M. Lam, H. So, C. Y. Chan, T. K. LI, C. C. Szeto, L. S. Tam
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> HT is the most prevalent comorbidity in axSpA (1), and is one of the strongest predictors for accelerated atherosclerosis and atherosclerotic vascular events in the general populations [2]. However, the association between time-varying inflammatory markers, disease activity and drug use and the development of incident hypertension (IHT) remain unknown. <h3>Objectives</h3> To elucidate the tiem-varying risk factors for the development of IHT in patients with axial spondyloarthritis (axSpA). <h3>Methods</h3> We conducted a long-term retrospective cohort study in axSpA patients who were recruited from 2001-2019 from a university clinic in Hong Kong. Patients with HT and/or anti-hypertensive drug use at baseline were excluded. They were followed until the end of 2020. The outcome was IHT, defined by a diagnosis and/or a prescription for an antihypertensive drug. Baseline and time-varying Cox regression analyses adjusting for age, sex, and body mass index (BMI), were used to assess the relationship between inflammatory burden, drug use and IHT. <h3>Results</h3> 413 patients [age: 34(25-43) years, male: 319 (77.2%)] were recruited. After a median follow up of 12 (6-17) years, 58 patients (14%) developed IHT (IHT+group). Among all the baseline variables, disease duration (BLDD) was the only independent predictor for IHT based on the Cox regression model. In the time-varying multivariate Cox regression analysis, ESR level as an inflammatory marker and BLDD longer than 5 or 10 years, remained as the significant independent predictors to increase risk of future IHT (Table 1a and 1b), while ESR≥20, the use of csDMARDs, sulfasalazine or paracetamol were no longer statistically significant. The Kaplan-Meier curve showed the survival probability were significant lower in groups with BLDD longer than 5 or 10 years (Figure 1). <h3>Conclusion</h3> Higher inflammatory burden as reflected by BLDD longer than 5 or 10 years were predictors associated with IHT after adjusting for inflammation marker and traditional CV risk factors. Higher ESR level may also play a role in the development of IHT in these patients. <h3>References</h3> [1]Zhao SS, Robertson S, Reich T, Harrison NL, Moots RJ, Goodson NJ. Prevalence and impact of comorbidities in axial spondyloarthritis: systematic review and meta-analysis. Rheumatology (Oxford). 2020;59(Suppl4):iv47-iv57. [2]Lawes CMM, Hoorn SV, Rodgers A. Global burden of blood-pressure-related disease, 2001. The Lancet. 2008;371(9623):1513-8. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
POS0674 RENAL SAFETY OF LONG TERM NSAID USE IN PATIENTS WITH ANKYLOSING SPONDYLITIS
Authors: Y. E. Kim, S. Y. Park, S. M. Ahn, S. Hong, C. K. Lee, B. Yoo, J. S. Oh, Y. G. Kim
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Nonsteroidal anti-inflammatory drugs (NSAIDs) are the basis of treatment for patients with ankylosing spondylitis (AS) to reduce pain and inflammation. However, long-term NSAID use may cause deterioration of renal function. <h3>Objectives</h3> We aimed to investigate the renal safety from long-term NSAID exposure in patients with AS. <h3>Methods</h3> We extracted clinical information from the electronic medical records of patients with newly diagnosed AS with an observation period of more than one year who were treated at Asan Medical Center from January 1, 2000, to December 31, 2020, excluding patients with chronic kidney disease Stage 4–5, known kidney disease, and malignancy. Renal function was determined by calcuation of the estimated glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease (MDRD) and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations. Patients were stratified into three groups according to initial GFR: Stage 1 (GFR≥90), Stage 2 (60≤GFR&lt;90), and Stage 3 (30≤GFR&lt;60). The GFR values for every 3-year interval were imputed by the linear interpolation method using the measured values before and after each point, and NSAID use in each interval was estimated as the medication possession rate (MPR). To evaluate the association between NSAID use and annual changes in GFR, linear mixed effects models were used and adjusted for key covariates including age, sex, body mass index, baseline GFR, relative dosage of NSAIDs, comorbidities, and comedications. <h3>Results</h3> Among 1,838 patients with AS, the mean age was 38.0 (SD, 13.8) years with a median 6.1 years of follow-up. The majority of 1,386 (75.4%) patients belonged to the Stage 1 group, and the number of patients in the Stage 2 and Stage 3 groups was 442 (24.0%) and 10 (0.5%), respectively. In the multivariable models, the mean annual decrease in GFR was significant (model 1: β=-0.684, 95% CI -0.980 to -0.389, p&lt;0.001; model 2: β=-0.387, 95% CI -0.770 to -0.004, p=0.048), and the MPR of NSAID use was significantly associated with an additional decrease in GFR (model 1: for 100% vs. 0% of MPR, β =-0.5, 95% CI, -0.8 to -0.1, p=0.008; model 2: for highest vs. lowest tertile of MPR, β=-0.519, 95% CI -0.906 to -0.132, p=0.009) in the Stage 1 group but not in patients in the Stage 2 group (Table 1). <h3>Conclusion</h3> This study suggested that long-term use of NSAIDs was associated with a small but significant decrease in GFR in patients with AS with normal initial renal function. <h3>References</h3> [1]Möller B et al. Chronic NSAID use and long-term decline of renal function in a prospective rheumatoid arthritis cohort study. Ann Rheum Dis. 2015 Apr;74(4):718-23. [2]Curhan GC et al. Lifetime nonnarcotic analgesic use and decline in renal function in women. Arch Intern Med. 2004 Jul 26;164(14):1519-24. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
POS0414 ASSOCIATIONS BETWEEN BONE MARROW ADIPOCYTE SIZE, BONE REMODELLING AND BODY MASS INDEX IN PATIENTS WITH BASE OF THE THUMB OSTEOARTHRITIS
Authors: M. Maniglio, L. Loisay, T. Hügle, J. Geurts
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Subchondral bone sclerosis, osteophyte formation and bone marrow lesions are radiographic hallmarks of base of the thumb osteoarthritis (CMC-1 OA)[1]. High body mass index (BMI) and obesity are major risk factors for CMC-1 OA [2]. Adipose tissue-derived systemic factors, such as lipids and adipokines, have been proposed as mediators of such increased risk at a non-weight bearing joint. In support of this hypothesis, alterations in systemic lipid levels have been found to partially associate with the severity of hand OA [3]. It is unknown whether subchondral marrow adipose tissue contributes to development and progression of CMC-1 OA. <h3>Objectives</h3> To determine whether bone marrow adipocyte (BMAd) size, as a surrogate marker of adipocyte lipolysis and (dys)function, differed as a function of the extent of subchondral bone remodelling and BMI in CMC-1 OA. <h3>Methods</h3> Trapezium bone resections were harvested from 14 consecutive CMC-1 OA patients (9 female, 63±11 years, 26±6 kg/m<sup>2</sup>) undergoing arthroplasty. BMAd size, osteoblast numbers and OA severity were determined by histomorphometry. Expression of the lipolytic enzyme monoacylglycerol lipase (MGLL) on bone marrow-resident cells was assessed by immunohistochemistry. <h3>Results</h3> Eight out of fourteen specimens displayed regions of increased bone remodelling and osteoblast numbers, which were classified by histology as subchondral sclerosis (<i>n</i>=6) and central osteophyte formation (<i>n</i>=2). BMAd size was significantly reduced (<i>p</i>=0.02) in the remodelling (839±319 μm<sup>2</sup>) compared with non-remodelling regions (1438±578 μm<sup>2</sup>), independent of OA severity. BMAd size was positively correlated with BMI (<i>r</i>=0.63, <i>p</i>=0.03), but in non-remodelling regions only. MGLL was differentially expressed both in terms of quantity and cell type in non-remodelling and remodelling regions (Figure 1). Surprisingly, MGLL was strongly expressed by osteoblasts and blood vessels rather than mature BMAd in remodelling regions. <h3>Conclusion</h3> Collectively, these data suggest that BMAd properties in the CMC-1 joint may be BMI-dependent. Increased lipolytic activity in subchondral bone marrow adipose tissue may be fueling pathologic bone formation in CMC-1 OA. <h3>References</h3> [1]van Beest <i>et al. Osteoarthritis Cartilage</i> 2018 [2]Rydberg <i>et al. RMD Open</i> 2020 [3]Loef <i>et al. Osteoarthritis Cartilage</i> 2022 <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
POS0372 GROUP-BASED TRAJECTORIES OF ADHERENCE TO ANTI-TUMOUR NECROSIS FACTOR (TNF) AGENTS: A POPULATION-BASED LONGITUDINAL STUDY
Authors: M. De Vera, E. C. Sayre, N. Rebić
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Studies of adherence to biologic disease modifying anti-rheumatic drugs (bDMARDs), namely anti-TNFs, have been largely limited to short durations or used traditional methods that do not capture the dynamic nature of medication taking. <h3>Objectives</h3> Our objective was to characterize long-term trajectories of adherence to anti-TNFs and evaluate associated factors. <h3>Methods</h3> We linked population-based health data on all physician visits, hospital admissions, and all dispensed medications, regardless of payer in British Columbia from 01/01/1996 to 3/31/2021. We identified prescriptions for anti-TNFs (including infliximab, etanercept, adalimumab) using drug identification numbers among indicated individuals (e.g., rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis) with at ≥6 years of continuous data following initiation. We used group-based trajectory models (GBTMs), a semi-parametric application of finite mixture modeling which detects longitudinal patterns in a repeatedly measured outcome, to identify and group individuals with similar patterns of bDMARD use (i.e., 'adherence trajectory group') over 6 years of follow-up. We then evaluated factors associated with each adherence trajectory group using multinomial logistic regression. <h3>Results</h3> We identified 1,593 patients prescribed anti-TNFs, of which 59.7% were female with a mean age of 45.2 ± 13.2 years. Group-based trajectory modeling identified 4 distinct adherence trajectories for anti-TNFs overall (<b>Figure 1a</b>): "moderate then high adherence" (Group 1; n = 814, 51.1% of the cohort), "moderate then low adherence" (Group 2; n = 314, 19.7%), "low adherence, declining to discontinuation" (Group 3; n = 291, 18.3%), and "low then high adherence" (Group 4; n = 174, 10.9%). Specific group-based trajectories for adalimumab, etanercept, and infliximab are presented in <b>Figure 1b-d</b>. Among anti-TNFs, number of prior hospitalizations was significantly associated with initial low adherence increasing to high adherence (Group 4) compared to initial moderate adherence increasing to high adherence (Group 1)(odds ratio 1.41; 95% confidence interval: 1.19, 1.68). <h3>Conclusion</h3> This population-based study demonstrates the heterogeneity in real-world patterns of anti-TNFs use. Findings also suggest the inadequacy of clinical and demographic characteristics in predicting patients' adherence trajectories. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
POS0771 JAK INHIBITORS AS TREATMENT OF ADULT PATIENTS WITH PEDIATRIC-ONSET JUVENILE IDIOPATHIC ARTHRITIS: A MONOCENTRIC EXPERIENCE
Authors: M. R. Pellico, M. Pandolfi, A. Marino, S. Costi, M. Cornalba, I. Pontikaki, M. Gattinara, R. Caporali, C. Chighizola
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> JAK inhibitors (JAKi), small molecules that inhibit the Janus kinase enzymes, are increasingly used to treat children with rheumatologic diseases. Clinical experience of JAKi in the management of adult patients with pediatric-onset rheumatic conditions is still scarce. <h3>Objectives</h3> The aim of this study consists in evaluating efficacy and safety of JAKi in a monocentric cohort of adult patients with juvenile idiopathic arthritis (JIA). <h3>Methods</h3> Clinical records of patients attending the rheumatology transition clinic at our centre were retrospectively reviewed; patients were included in case of: i) JIA diagnosis according to current classification criteria (1); ii) age ≥18 years and iii) treatment with JAKi for at least 3 months. <h3>Results</h3> 17 patients that met the inclusion criteria were included in this study. Their demographics and clinical features are detailed in <b>Table 1</b>. 9 patients were treated with tofacitinib (52.9%) and 8 subjects (47.1%) received baricitinib. At 3 months, 4 patients (23.5%) achieved disease remission on JAKi: 3 patients achieving remission were treated with baricitinib and 1 with tofacitinib (37.5 vs. 16.7%, p=0.29). None of the patients with systemic JIA and enthesitis-related arthritis obtained remission; the remission rate at 3 months was higher, although not significantly, in the oligoarticular subset compared to the polyarticular subset (37.5 vs. 20%; p=1.0). Disease duration, age at onset and at JAKi start were similar between patients achieving remission and those with active disease (p=0.94, p=0.58 and p=0.72, respectively). Patients with ≤1 active joint involvement at JAKi start had higher remission rate (50 vs. 22.2%; p=0.58). Subjects who achieved remission on JAKi had a significantly lower pre-treatment DAS28 compared to those with still active disease (median DAS28 (IQR) 2.17 (1.9-2.4) and 4.54 (3.8-4.9), respectively; p=0.01, Mann-Whitney U=4). A pre-treatment DAS28 &lt;3.76 predicted response to JAKi with 100% sensitivity and 84.6% specificity (AUC 0.88, p=0.02, 95%CI 0.71-1.05). Concomitant treatment with methotrexate did not significantly affect the remission rate (16.7 vs. 37.5%; p=1.0). This was lower among patients who had been treated with ≥2 biological drugs before JAKi start (9 vs. 66.7%; p=0.05). None of the patients developed side effects during JAKi treatment. <h3>Conclusion</h3> JAKi could represent an effective and safe treatment option for adult JIA patients with low/moderate disease activity, particularly in case of oligoarticular involvement. <h3>Reference</h3> [1]Petty RE, International League of Associations for Rheumatology classification of juvenile idiopathic arthritis: second revision, Edmonton, 2001. J Rheumatol 2004;31:390–2. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
POS0744 MULTISYSTEM INFLAMMATORY SYNDROME IN CHILDREN ACROSS 16 LATIN AMERICAN COUNTRIES: A MULTICENTER STUDY FROM THE REKAMLATINA NETWORK
Authors: J. Garcia-Silva, R. Ulloa-Gutierrez, G. Ivankovich Escoto, M. A. Yamazaki-Nakashimada, E. Faugier Fuentes, O. Del Águila, A. V. Villlarreal, G. Camacho Moreno, D. Estripeaut, I. F. Gutiérrez, D. Castillo-Bustamante, K. Luciani, M. Fabi, G. Espada, A. Pringue, M. I. Álvarez-Olmos, C. Silfa, M. García-Domínguez, P. Pérez-Camacho, S. Duarte-Passos, K. L. Borjas Aguilar, M. C. Cervi, R. O. Martínez-Ramírez, E. M. Cantillano, B. A. Llamas-Guillén, M. Velázquez-Méndez, P. Saltigeral-Simental, J. Criales, A. H. Tremoulet, T. Rekamlatina- Mis-C Study Group Investigators
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Multisystem Inflammatory Syndrome in Children (MIS-C) is one of the most feared complications following SARS-CoV2 infection in children and adolescents. Few multinational multicenter studies from Latin America have been published. <h3>Objectives</h3> To describe the clinical presentation, management, and outcomes of MIS-C in Latin America. <h3>Methods</h3> Observational, prospective and retrospective, multicenter study to gather information from 84 participating centers across 16 Latin American countries, between August January 1, 2020 and June 30, 2022. <h3>Results</h3> Of the 1,239 reported cases of MIS-C, 84.2% were previously healthy. The most frequent clinical manifestation in our studied population was abdominal pain (N=804, 64.9%), followed by conjunctival injection (N=784, 63.3%). The median days of fever at the time of hospital admission was 5 and a significant number of subjects required admission to an intensive care unit (N=589, 47.8%). A total of 538 (47.2%) patients had an abnormal initial echocardiogram. Most of the subjects (N= 1,096, 88.7%) were treated with intravenous immunoglobulin (IVIG), while 76.7% (N= 947) were treated with steroids, of which 10.6% (N= 100) did not receive IVIG. The death rate attributed to MIS-C was 4.88%, with a rate of 3.39% for those initially diagnosed with MIS-C and 8.85% for those whose admission diagnosis was not MIS-C (<i>P= 0.00001</i>). <h3>Conclusion</h3> One of the most significant findings from our study was the death rate, especially in those not initially diagnosed with MIS-C, in whom it was higher. This highlights the importance of increasing awareness and making an earlier diagnosis of MIS-C in Latin America. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
POS0758 ON DEMAND CANAKINUMAB THERAPY FOR COLCHICINE RESISTANT FAMILIAL MEDITERRANEAN FEVER (FMF) PAEDIATRIC PATIENTS – A MULTICENTER STUDY
Authors: K. Shehadeh, Y. Levinsky, R. Tal, S. Kagan, T. Zoabi, L. Harel, G. Amarilyo
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Familial Mediterranean fever (FMF) is the most common autoinflammatory disease. Without therapy, it may lead to the development of secondary amyloidosis. Treatment with colchicine leads to long-term remission in ~70% of patients. 5% are resistant to colchicine therapy (crFMF) and may be treated with monthly dose of canakinumab (anti IL-1beta). However, colchicine, the only drug proved to prevent secondary amyloidosis. Canakinumab is immunosuppressive as well as expensive. <h3>Objectives</h3> To compare on demand canakinumab (COD) dosage policy vs. canakinumab fixed frequency (CFF) policy. <h3>Methods</h3> Data from 3 pediatric rheumatology centers (Schneider, Sheba, Rambam) were collected regarding crFMF patients treated with canakinumab. crFMF patients treated according to the COD policy were given 1 dose of sc-canakinumab injection 4mg/kg (max 150mg), with subsequent doses administered only after an additional attack. CFF patients were given fixed 4 weekly doses according to the manufacturer instructions. <h3>Results</h3> Overall, 51 crFMF (25 COD vs. 26 FCC) with mean follow-up of 22.6 months were included. There were no significant demographic, clinical or genetic differences between the groups. The COD group received significantly lower cumulative canakinumab dosage during the follow-up period (15.68±8.95mg/kg vs.32.5±8.05mg/kg;P&lt;0.001). There were no differences between groups in mean FMF attacks nor in mean CRP levels at the end of follow-up period. None the less, the COD group necessitated higher colchicine doses (0.05±0.01mg/kg vs. 0.03±0.01mg/kg;P&lt;0.001). <h3>Conclusion</h3> COD treatment in crFMF patients is as effective as CFF treatment. Using COD can reduce drug expenses and decrease immunosuppression exposure without negatively influencing the disease control. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
POS0629 DIFFERENT GUT MICROBIOME PROFILES AMONG PATIENTS WITH SYSTEMIC SCLEROSIS COMPARED TO RHEUMATOID ARTHRITIS
Authors: Y. Braun-Moscovici, N. Asulin, K. Dolnikov, V. Shataylo, S. Giryes, D. Markovits, R. Erlich, K. Toledano, Y. Tavor, A. Balbir-Gurman, O. Koren
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> A growing body of evidence suggests that the gut microbiota plays a significant role in the development of autoimmune diseases. An altered microbiota composition has been associated with gastrointestinal and extraintestinal features in systemic sclerosis (SSc) patients. <h3>Objectives</h3> To characterize differences in the gut microbiota between SSc patients and rheumatoid arthritis (RA) patients and to look for associations between microbial profiles and SSc subtypes, disease manifestations and treatment. <h3>Methods</h3> SSc and RA patients seen at our center were recruited in a prospective study. The exclusion criteria included antibiotic or probiotic treatment during the month prior to recruitment, recent hospitalizations, BMI&gt;30, diabetes mellitus or concomitant inflammatory bowel disease. Fecal samples were collected and processed and 16S rRNA gene sequences were analyzed using the QIIME2 package. Microbiome composition was determined, beta diversity and alpha diversity were calculated and ANCOM analyses was performed. <h3>Results</h3> During 7/2018-4/2022, 49 SSc patients (mean age [SD] 53.5[13.8] and disease duration 9.4 [8.0] years) and 21 RA patients (mean age [SD] 57.1[10.4] and disease duration 15.1[10.0] years) fulfilled the criteria and were willing to participate in the study. Significant differences in beta diversity (Unweighted q=0.019, and Weighted UniFrac q=0.005) were found between RA and SSc patients' stool microbiota, but not in alpha diversity. Composition analysis revealed higher abundance of Actinomyces and relative paucity of Coprococcus Eutactus among SSc patients compared to RA. Significant variations in beta diversity (unweighted and weighted) were associated with the subtype of SSc (diffuse - 27 vs limited - 22 patients, p [weighted] = 0.01), occurrence of interstitial lung disease (22 patients, p=0.011), renal crisis (3 patients, p=0.016), immunomodulatory treatment (33 patients, p=0.018) and biological treatment (11 patients, p=0.017). Composition analysis revealed higher relative abundance of Firmicutes in patients with GAVE [12]. Patients on biologicals (11) had higher abundance of Synergistaceae and lower of Firmicutes. The changes were consistent in recurrent fecal samples. <h3>Conclusion</h3> Significant differences on beta diversity were found between RA and SSc patients' gut microbiota, but not on alpha diversity. Diffuse SSc, interstitial lung disease, renal crisis and immunomodulatory treatment were associated with shifts in the microbiome of SSc patients. The impact of these changes on SSc disease progression needs further elucidation. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.